{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:57:37Z","timestamp":1791295057899,"version":"4.1.0"},"reference-count":55,"publisher":"The Company of Biologists","issue":"24","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,12,15]]},"abstract":"<jats:p>Autosomal dominant Emery-Dreifuss muscular dystrophy is caused by mutations in the LMNA gene, which encodes lamin A and lamin C. Mutations in this gene also give rise to limb girdle muscular dystrophy type 1B, dilated cardiomyopathy with atrioventricular conduction defect and Dunnigan-type partial lipodystrophy. The properties of the mutant lamins that cause muscular dystrophy, lipodystrophy and dilated cardiomyopathy are not known. We transfected C2C12 myoblasts with cDNA encoding wild-type lamin A and 15 mutant forms found in patients affected by these diseases. Immunofluorescence microscopy showed that four mutants, N195K, E358K, M371K and R386K, could have a dramatically aberrant localization, with decreased nuclear rim staining and formation of intranuclear foci. The distributions of endogenous lamin A\/C, lamin B1 and lamin B2 were also altered in cells expressing these four mutants and three of them caused a loss of emerin from the nuclear envelope. In the yeast two-hybrid assay, the 15 lamin A mutants studied interacted with themselves and with wild-type lamin A and lamin B1. Pulse-chase experiments showed no decrease in the stability of several representative lamin A mutants compared with wild-type. These results indicate that some lamin A mutants causing disease can be aberrantly localized, partially disrupt the endogenous lamina and alter emerin localization, whereas others localize normally in transfected cells.<\/jats:p>","DOI":"10.1242\/jcs.114.24.4435","type":"journal-article","created":{"date-parts":[[2021,4,26]],"date-time":"2021-04-26T00:33:11Z","timestamp":1619397191000},"page":"4435-4445","source":"Crossref","is-referenced-by-count":174,"title":["Properties of lamin A mutants found in Emery-Dreifuss muscular dystrophy, cardiomyopathy and Dunnigan-type partial lipodystrophy"],"prefix":"10.1242","volume":"114","author":[{"given":"Cecilia","family":"O\u0308stlund","sequence":"first","affiliation":[{"name":"Departments of Medicine and of Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gise\u0300le","family":"Bonne","sequence":"additional","affiliation":[{"name":"INSERM UR523, Institut de Myologie, GH Pitie\u0301-Salpe\u0301trie\u0300re, 75651 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ketty","family":"Schwartz","sequence":"additional","affiliation":[{"name":"INSERM UR523, Institut de Myologie, GH Pitie\u0301-Salpe\u0301trie\u0300re, 75651 Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard J.","family":"Worman","sequence":"additional","affiliation":[{"name":"Departments of Medicine and of Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","reference":[{"key":"2021042600082027700_AEBI-ETAL-1986","doi-asserted-by":"crossref","unstructured":"Aebi, U., Cohn, J., Buhle, L. and Gerace, L. 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